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Endothelial dysfunction in congestive heart failure: ACE inhibition vs. angiotensin II antagonism
Author(s) -
Schäfer Andreas,
Fraccarollo Daniela,
Tas Piet,
Schmidt Isabel,
Ertl Georg,
Bauersachs Johann
Publication year - 2004
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2003.10.009
Subject(s) - irbesartan , trandolapril , medicine , heart failure , endothelial dysfunction , angiotensin ii , ace inhibitor , angiotensin ii receptor antagonist , enos , vasodilation , endothelium , endocrinology , cardiology , angiotensin converting enzyme , angiotensin receptor , nitric oxide , receptor , nitric oxide synthase , blood pressure
Background: Endothelial dysfunction of the vasculature contributes to the elevated peripheral resistance and reduced myocardial perfusion in congestive heart failure (CHF). The present study systematically investigated the effect of angiotensin II (AT 1 )‐ receptor blockade on vascular superoxide (O 2 − ) production and endothelial dysfunction. Methods and results: Vasodilator responses and O 2 − production were determined in aortic rings from Wistar rats with experimental CHF 10 weeks after extensive myocardial infarction and compared with sham‐operated animals (Sham). Rats were either treated with placebo (P), with the AT 1 ‐receptor antagonist Irbesartan (50 mg kg −1 day −1 ) or with the ACE inhibitor Trandolapril (0.3 mg kg −1 day −1 ). In CHF‐P, endothelium‐dependent, acetylcholine‐induced relaxation was significantly attenuated compared with Sham‐P. Chronic treatment with Trandolapril or Irbesartan significantly improved endothelium‐dependent relaxation. Aortic O 2 − formation was markedly increased in CHF, and was not significantly affected by Trandolapril treatment, while it was reduced by Irbesartan. eNOS expression was reduced in CHF and normalised by both treatments. Conclusion: Endothelial vasomotor function in CHF rats was normalised by long‐term treatment with an ACE inhibitor or an AT 1 ‐antagonist. Reduced aortic eNOS expression was normalised by both treatments, whereas aortic superoxide formation was only reduced by the AT 1 ‐antagonist Irbesartan.